Two-dimensional echocardiography in experimental coronary stenosis. II. Relationship between systolic wall thinning and regional myocardial perfusion in severe coronary stenosis.
To determine if there is a quantitative relationship between systolic contraction abnormalities (demonstrated by two-dimensional echocardiography) and reduced myocardial perfusion in a setting of moderate and severe coronary stenosis, we created 70% or 90% reduction in circumflex coronary artery diameter in open-chest dogs. Transient ischemia was induced by superimposing increased myocardial oxygen requirements (i.v. isoproterenol, aortic constriction) in the presence of the stenosis or by decreased coronary perfusion (lowering arterial pressure with i.v. nitroprusside, nitroglycerin, or hemorrhage). Acute systolic wall thinning show by two-dimensional echocardiography or by implanted myocardial sonomicrometers was taken as functional evidence of myocardial ischemia. Myocardial perfusion was determined by radiolabeled microspheres when wall thinning was apparent. Systolic wall thinning could not be induced by these interventions when the degree of coronary stenosis was only 70%. Systolic wall thinning occurred only when increased myocardial oxygen requirements or decreased aortic pressure were superimposed on 90% coronary stenosis. Under these conditions, myocardial perfusion was reduced to 28 +/- 27 ml/100 g/min (mean +/- SD), 15--25% of control. Aortic diastolic pressure was a major determinant of ischemia in that contraction abnormalities produced by a 90% stenosis and vasodilators or hemorrhage could be acutely reversed by superimposing acute aortic constriction, which elevated arterial pressure; myocardial perfusion increased correspondingly. Thus, the demonstration of transient systolic wall thinning by two-dimensional echocardiography during a stressful intervention indicated that severe coronary stenosis was present, and that the perfusion of the acutely dyskinetic myocardial area was 25% of control or less.
D000818:Animals; D003251:Constriction, Pathologic; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D004452:Echocardiography / Q000379:methods; D007545:Isoproterenol / Q000494:pharmacology; D008863:Microspheres; D009200:Myocardial Contraction; D005996:Nitroglycerin / Q000494:pharmacology; D010477:Perfusion; D013599:Systole
D005996:Nitroglycerin; D007545:Isoproterenol